Sounded really weird to me to be honest...that is why I was curious and wanted to read it since it just came out like a few days ago and I haven't read anything recent on MAP. Yet, it is no where to be found...except if you pay which I wont do.

And you are right, the certainty in the title based on correlation between Milk consumption (only) is odd.

I presume he wouldn't say that because he's trying to sound scientific. Scientific findings are usually reported in understated, cautious language. Use of over-the-top superlatives and exaggerations is the language of quacks and charlatans.

The fact that the Qin piece has only one author and no abstract makes me wonder whether it is an opinion piece or editorial, or maybe a review, rather than report of new data.

That's what I was wondering, but there is no way to know. And if it is an opinion piece, it would still be a strange way to state the title almost with certainty without data to validate. I would be interested in reading it though.

I've heard this basic argument before, which is "If MAP is in milk, why do those who drink more milk have less CD?" I think there's an old study about that, but the basic answer is that MAP won't do a thing to you unless you have the genetic predisposition to not allow your immune system to recognize intracellular infections and also a triggering event, like stress, a loss of someone close, Vit D deficiency, the flu, antibiotic use, some other environmental exposure that no one knows about yet. So a great study would be to only look at patients with IBS or those with the genetic predisposition for CD, randomize a huge group of them, then make half consume dairy and the other half stay away from it completly - for like 10 years. And then see which group develops higher incidence of CD. So you can see it's completely impractical. Milk isn't the only issue going on with CD. There are a whole chain of issues, and the increased MAP in milk due to more herds being infected (and especially infant formula) may result in a higher level of MAP exposure at a younger age, therefore precipitating higher CD rates in those genetically susceptible. Dr. Collins talked about this at the symposium. And it's just a theory right now.

I was trying to get this paper any way possible, but it's published in e-print ahead of the Sept. 22nd journal publication. Also, it looks like this journal is the publication of the CCFA, so it may be a bit biased, since they seem to dislike the MAP theory of CD. If I can get it, I'll let you know! Reserving judgment until I read it.

__________________
Currently on: Anti-MAP therapy and loving life! Full remission since Jan 2015. Clarithromycin, rifampin and low dose naltrexone. (Levofloxicin had too many side effects so discontinued after 5 months.) Resources on human MAP and Crohn's here: HumanPara.org.

Past (failed) Treatments: Remicade, Humira, Prednisone, Pentasa, Azulfadine, Lialda, No gluten/dairy/sugar/coffee or processed food in general. Flagyl worked but not long term.

The quote below is taken from Dr. Qin's LinkedIn page and spells out his theory of the cause of IBD. Presumably he views MAP as a competing theory.

" Engaged in medical research in the academic for more than twenty years. More than a decade ago, a series of accidental findings made him suspect that impaired inactivation of digestive proteases due to the reduction in gut bacteria along with improved hygiene and inhibition by some dietary chemicals may have played important causative role in inflammatory bowel disease (IBD, including ulcerative colitis and Crohn's disease), which emerged and dramatically increased in last century. During the last decade he published a series of papers and proposed that damage of gut by the poorly inactivated digestive proteases may be the root cause of IBD. Not only IBD, more and more studies revealed many other diseases that are dramatically increasing in modern society, such as irritable bowel syndrome (IBS), multiple sclerosis, type I and type II diabetes, asthma, atopic eczema/ dermatitis, obesity, autism, etc, all accompanied by increased gut permeability, suggesting damage of gut barrier would have also contributed to the development of these diseases. He recently started a company, GI Biopharma Inc, with the goal to develop new treatments for these diseases."

J Crohns Colitis. 2016 Aug 23. pii: jjw148. [Epub ahead of print]
Inflammatory bowel disease incidence is on the continuous rise among all pediatric patients except for the very young - a nationwide registry-based study on 28-year follow-up.
Virta LJ1, Saarinen MM2, Kolho KL3.
Author information
Abstract
BACKGROUND AND AIMS:
The burden of inflammatory bowel disease (IBD) in health care is high. We conducted research on the temporal changes in the incidence of pediatric IBD (PIBD) using nationwide registry-based data in Finland.
METHODS:
All PIBD cases diagnosed at less than 20 years of age during 1987-2014 (in total, 5,415 patients) were retrieved from a database documenting reimbursements for drug costs. Incidence rates were calculated by dividing the number of annual new PIBD cases by the size of the pediatric population at risk during each calendar year. Temporal trends in the incidences of PIBD and its subtypes, ulcerative colitis (UC) and Crohn's disease (CD), were estimated using Poisson regression analyses.
RESULTS:
The mean annual incidence of PIBD increased from 7/100,000 for the years 1987-1990 to 23/100,000 for the years 2011-2014. The average rate of increase was 4.1% (95% CI: 3.6-4.5) per annum. In the period 2000-2014, the increase rate in the annual incidence of UC (3.8%; 95% CI: 2.7-5.0), was steeper than for CD (2.5%; 95% CI: 1.0-3.8). The most pronounced increase occurred in UC among adolescents aged 16-19 years: 4.8% (95% CI: 2.9-6.7). For children less than 10 years of age, the rate of change remained low. Approximately 0.17% of the birth cohort for the years 1999-2000 was diagnosed with PIBD by the age of 14 years.
CONCLUSION:
The incidence of PIBD is primarily increasing among adolescents, challenging the identification of the possible environmental triggers for the disease.

Very interesting article:
Dig Liver Dis. 2016 Aug 5. pii: S1590-8658(16)30546-1. doi: 10.1016/j.dld.2016.07.036. [Epub ahead of print]
Occupational risk for Crohn's disease: A two-center study.
Liu S1, Ding J1, Wang M1, Wang G2, Wu X2, Feng M1, Song P1, Ren J3, Guan W4.
Author information
Abstract
BACKGROUND:
Occupational factors have been suggested as possible elements in the etiology of Crohn's disease, although evidences have not been fully obtained.
AIMS:
This study is to investigate possible associations between occupation and development of Crohn's disease.
METHODS:
This prospective study was carried out in two major hospitals during January 2010 and December 2014. Demographic and clinical data were collected for the calculation of standard incidence ratios and 95% confidence intervals by occupation.
RESULTS:
A total of 401 patients with Crohn's disease were recruited into this study. Participants were distributed into 8 major occupational groups, among which "professionists" (17.7%), "service and sales" (18.7%) and "unclassified individuals" (mainly students) (20.2%) took up the most proportions. Increased standard incidence ratios were found in "service and sales" (2.526±0.135, 95% CI: 1.939-3.290), "professionists" (4.216±0.142, 95% CI: 3.194-5.565), and most significantly, in "administrative staffs" (5.476±0.170, 95% CI: 3.926-7.639). In contrast, decreased standard incidence ratios for Crohn's disease were observed in the category of "workers in agriculture, forestry, animal husbandry, fishery and water conservancy" (0.088±0.146, 95% CIs: 0.066-0.117).
CONCLUSION:
Occupational elements are implicated in the likelihood of development of Crohn's disease.

Scared - I wonder if more active professions have less incidence than more sedentary desk jobs because exercise has been shown to help CD? Also thinking that the stress factor of office life may play a role too. The poor admins! Will have to read the whole thing.

Scared - I wonder if more active professions have less incidence than more sedentary desk jobs because exercise has been shown to help CD? Also thinking that the stress factor of office life may play a role too. The poor admins! Will have to read the whole thing.

That could be a contributing factor - who knows, maybe these active professions may have the incidence but it is under control and they are not diagnosed? but its interesting they all have to do with exposure of some kind to "nature" and consequently, could be related to healthier microbiome? I am not sure...it is really interesting all this research though, but I have yet to see one that talks about how there are different types of crohn's in the sense - MAP associated, AEIC associated...etc...

I remember seeing that too...just like the map vaccine delay...but its either they saw negative results and want to dig in more to see why it didnt have the effect (they said they wanted to learn more about the patient population), or they had great results (but why would they not want to publish as soon as possible), so I am worried that this might be not a pro map sotuation I don't think that would really hurt the map crohns link. But, if there wasn't a link, how could they discount the obvious benefit it gave come people? I mean, its not a massive placebo that has worked on so many...I just wish some validation would come about already. I really believe that if it were the cauae (and I do believe it is for many), that a study like this could get more buy in and more people involved in finding a permanent solution to this mystery.

It may be they aren't able to recruit enough patients. I think in June they had met only 75% of their recruitment goal for this study (200 out of 270). The study has 26 weeks of treatment, plus evaluation of duration/maintenance of remission at 52 weeks. I don't know how all this plays into the delays, but it's one explanation.

Here's from their Aug. 11th Semi annual research report. Looks like they want to get full enrollment, and they are considering some type of US protocol change. But the key thing is that RedHill apparently still remains blinded, so they can't be increasing the timelines because it either works/doesn't work, which I see as good news. I'd rather them take their time and get it right than rush and have another unreliable study, but yes, it's SOOO hard to wait! Especially when GIs will be more likely to prescribe AMAT once results are released. I was hoping for that in Nov. 2016, but I guess it will be Sept. 2017.

Approximately 200 subjects out of the planned total of 270 have been enrolled to date in the randomized, double-blind, placebo-controlled first Phase III study with RHB-104 for Crohn’s disease (the MAP US study).

Interim data and safety monitoring board (DSMB) analysis is on track to take place in the fourth quarter of 2016 and RedHill remains blinded to the interim and ongoing results.

RedHill is currently reviewing a possible amendment to the Phase III MAP US study protocol intended to further enhance the overall robustness of the study, provide a more precise assessment of RHB-104’s treatment effect, collect additional endoscopic mucosal healing data, further evaluate the Crohn’s disease population enrolled and address retention and early terminations. No changes are planned to the primary endpoint of remission at week 26 or the study’s 90% power. Taking into account a potential protocol amendment, completion of recruitment is expected in 2017 with no anticipated material impact on the Company’s overall cash burn rate through the end of 2017. The Company expects to provide further details in the coming weeks, once plans are finalized.

Does anyone here know if doctors in the US risk having their license revoked by treating Crohn's with AMAT? After watching Under Our Skin, about Lyme disease and what happened to some doctors who went against protocol, I was wondering if there is the same risk.

So far I haven't heard of any, though I imagine it's a concern to many. I haven't watched the piece on Lyme's, but there's some really decent research and small study data which could justify treatment of CD with AMAT, so that would be in their favor. Also, patients who don't have traditional treatment options left may be more able to get AMAT due to that. I volunteered to my doc that I'd be happy to sign an informed consent and liability waiver, since it would protect her a slight bit more. She only saw it as a formality, since she thiught the research was valid and due to that wasn't worried about the liability. I think the argument could be made that the RedHill trial (being in stage 3 with promising previous stage data) would insulate docs who decide to follow that protocol. At the end of the day though, it's not an approved treatment pathway, and without the large double blinded study, I think docs are more worried about success and risk to the patient vs. the liability issue to themselves. At this point, they just aren't convinced it works.

(Of course, if RedHill turns out successful, starting a tidal wave of funding on research into this theory which eventually conclusivelyproves CD to be zoonotic, there's going to be liability assessed then too. Who knew what, when did they know, why wasn't research funded, etc. But that's a whole different issue!)

In this retrospective study, the researchers are theorizing that TB induces an auto-immune reaction to trick the immune system into attacking the lungs which in turn helps its transmission: "...autoimmunity is a critical process exacerbating pathology in TB, leading to cavitation and transmission."

They support their theory by listing diverse autoimmune phenomena that occur in a portion of TB cases. For example, autoantibodies associated
with diseases such as Wegener's granulomatosis and systemic lupus erythematosus is detected in 40% of TB patients. They also point to cases of uveitis and erythema nodosum, which also occurs in some TB cases. Their strongest argument is that TB and Sarcoidosis, an autoimmune disease with no proof of an infectious etiology, are virtually indistinguishable.

Even though this is a theory they've got, given TB and MAP are cousins, this may have some interesting implications for MAP research, at least from a layperson's perspective.

As someone who is aware of the theory of MAP being associated with causing Crohn's, but not well read, and someone with fistulas, I was wondering if anyone knew why they would exclude these patients from the trial? Mainly I am thinking for the future (if this treatment was proved effective is there something about having a fistula that prevents anti-MAP therapy as an option)?

Not sure if it's something that anyone is going to have an answer for, but I figured it's probably not something I am going to find in a frequently asked questions somewhere regarding the trial.

My son could not participate for the same reason, and I inquired as to why because AMAT is effective for healing fistulas. The only reason why they exclude fistulas is that having them is considered a separate disease, called Fistulizing Crohn's! Trials are very strict with their criteria and researchers cannot deviate at all from them otherwise they will not get approval. It is very frustrating but unfortunately it is how the process works.

I have faith that it will win approval though...at least I hope so, and at that time you should be able to get on the treatment.

My son could not participate for the same reason, and I inquired as to why because AMAT is effective for healing fistulas. The only reason why they exclude fistulas is that having them is considered a separate disease, called Fistulizing Crohn's! Trials are very strict with their criteria and researchers cannot deviate at all from them otherwise they will not get approval. It is very frustrating but unfortunately it is how the process works.

I have faith that it will win approval though...at least I hope so, and at that time you should be able to get on the treatment.

Thanks, it's interesting, but it doesn't say they've made a vaccine, it says:

Davis’ theory linking Crohn’s disease to MAP infections in humans, has driven him to devote a significant part of his career to the development of a vaccine to remove MAP from cattle, and thus from the food supply and the environment.
Regardless of whether or not MAP is causative, “We’re making significant progress on a vaccine,” explained Davis. A cattle vaccine provides the greatest promise for controlling Johne’s disease and benefitting cattle, regardless of the uncertainty surrounding the associations to human Crohn’s disease.

Edit: On second thought, semantically, it's not wrong to infer that they have made a vaccine. My bad. I can't delete this post so I'm editing it instead.

Dr. Prabhat Agarwal took interest in the case and was willing to consider the patient’s illness could be associated with an extensive infection with MAP. Dr. T. J. Borody, who had reported success in treating patients with CD with antibiotics was contacted for advice and recommendation on how to treat the patient (7). Dr. Borody provided copies of recent publications and suggested what antibiotics should be considered for treatment. Based on his suggestions, a regimen of therapy was designed and implemented. The patient was informed that his clinical symptoms were most likely caused by a MAP infection and that a regimen of antibiotic therapy might provide a cure. After obtaining his written consent, he was placed on anti-MAP therapy under the supervision of Dr. Prabhat Agarwal. The antibiotic therapy included clarithromycin, rifampin, ethambutol, levofloxacin, isoniazid, and rifaximin along with mesalazine according to the schedule in Table 1.

Results
After 4 months of treatment, the patient exhibited improvement in his physical condition, reduction in stool frequency (two to three times a day from every half hour), and improvement in appetite. During the last months of treatment, the patient experienced continued improvement, with an increase in weight and further reduction in stool frequency (one to two times a day). Recovery from infection was complete following a year of treatment with no signs or symptoms of disease. The follow-up stool microscopy was negative for MAP (Figure 2B) and the follow-up post-treatment stool culture was negative for MAP. As mentioned, biotyping of colonies from cultures of stool showed the bacilli were the “Indian Bison type” of MAP (Figure 3). The ELISA was positive for MAP also, further confirmation that the patient had been infected with MAP (Table 2). The patient is now being monitored every 6 months for recurrence of infection and general health.

This case provides additional evidence, supporting studies showing MAP is the causative agent in, at least, a subset of patients with CD (26) and that antibiotic therapy may lead to a cure of CD and clearance of infection with MAP. The results are consistent with findings from a group of MAP infected patients treated successfully by one of the coauthors, Dr. J. Todd Kuenstner, in the United States using a regimen of multi-antibiotic therapy combined with ultraviolet blood irradiation (UVBI) (27, 28). Of major importance, the results obtained in this report and the mass survey in India emphasize the need for recognition, at the international level, that MAP is a zoonotic pathogen and that it is a health risk for humans and livestock (29).

In layman's terms, take a group of patients with identical symptoms who live in an area of the world where Tuberculosis is prevalent, but Crohn's is also present. Treat them with anti-Tuberculosis antibiotics and observe their symptoms at regular intervals up to 12 months. The outcome? They roughly divide into three groups:
1) The group with Mycobacterium Tuberculosis infection who recover completely -> ITB
2) The group where their general symptoms improve but they are not cured and they do not achieve mucosal healing -> Crohn's probably caused by MAP
3) The group who show no improvement or their symptoms get worse -> Crohn's caused by ?

The important point though is this, what we call Crohn's has identical symptoms to another mycobacterial infection intestinal Tuberculosis, the only difference is the antibiotics used to treat TB do not kill it off. Further, the group we label as Crohn's has two clear sub-groups based on how they respond to antibiotics, one of which I believe is a MAP infection.

AIEC is probably the other culprit imo, lots of literature stacking up suggesting so, also seems to be a few therapies targeting AIEC in the works... hopefully between the map vaccine and qu biologic's ssi vaccine we can say goodbye to this horrible condition.